A major pathogenic mechanism contributing to vascular pathology in atherosclerosis, hypertension resulting from renal artery stenosis and other causes, restenosis of coronary and other arteries after coronary angioplasty, insertion of vascular stents or due to non-angioplasty injury to blood vessels and proliferative diabetic retinopathy, is vascular hyperplasia, i.e., the excessive proliferation and hypertrophy of vascular smooth muscle cells. Vascular hyperplasia leads to thickening of the arterial wall, narrowing of the vascular lumen and, ultimately, interruption of organ blood flow and tissue death. Currently, treatments are invasive or are directed at complications. Treatments with agents which are non-toxic and non-invasive to inhibit the initiation and/or progression of vascular hyperplasia would be of great benefit.